1-7 studies, correlations have been based primarily on estimates of fiber intake obtained by grouping foods according to their fiber content. In the only case-control study and the only correlation study in which total fiber consumption was quantified rather than estimated from the consumption of high fiber foods, no association was found between high fiber intake and a lower risk of colon cancer. However, the correla- tion study indicated that the incidence of colon cancer was inversely related to the intake of one fiber component—the pentosan fraction, which is found in whole wheat products and other food items. Laboratory experiments also have indicated that the consumption of some high fiber ingredients (e.g., cellulose and bran) inhibits the in- duction of colon cancer by certain chemical carcinogens. However, the results are inconsistent. Moreover, they are difficult to equate with the results of epidemiological studies because most laboratory investi- gations have focused on specific fibers or their individual components, whereas most epidemiologlcal studies have been concerned with fiber- containing foods whose exact composition has not been determined. Thus, the committee found no conclusive evidence to indicate that dietary fiber (such as that present in certain fruits, vegetables, grains, and cereals) exerts a protective effect against colorectal cancer in humans. Both epidemiologlcal and laboratory reports suggest that if there Is such an effect, specific components of fiber, rather than total fiber, are more likely to be responsible. Vitamins In recent years, there has been considerable interest in the ,role of vitamins A, C, and E in the genesis and prevention of cancer. In con- trast, less attention has been paid to the B vitamins and others such as vitamin K. Chapter 9 contains more detailed information on the evidence summarized below. Vitamin A. A growing accumulation of epidemiological evidence indi- cates that there is an inverse relationship between the risk of cancer and the consumption of foods that contain vitamin A (e.g., liver) or its precursors (e.g., the carotenoids in green and yellow vegetables). Most of the data do not show whether the effects are due to carotenoids, to vitamin A itself, or to some other constituent of these foods. In these studies, investigators found an inverse association between estimates of "vitamin A" Intake and carcinoma at several sites, e.g., the lung, the urinary bladder, and the larynx. Studies in laboratory animals indicate that vitamin A deficiency generally increases susceptibility to chemically Induced neoplasia and that an Increased intake of the vitamin appears to protect against car- cinogenesis In most, but not all cases. Because high doses of vitamin A are toxic, many of these studies have been conducted with its synthetic